The present disclosure generally relates to systems and methods for minimizing formation of blood clots. More particularly, it relates to non-pharmacological systems or device/drug combination systems and methods for preventing blood clot formation in a chamber of a patient's heart or at other anatomical locations, for example preventing atrial thrombi in the left atrium of patients suffering from atrial fibrillation.
Stagnant blood can result in a clot, which is known as a thrombus, while it is immobile at its place of origin. If the clot becomes mobile and is carried away by the blood circulation, it is called an embolus. An embolus proceeds through smaller and smaller arteries until it plugs one of them and prevents blood from flowing any further in that artery. The result can be damage to tissue, and can occur in various parts of the body depending on where the embolus resides. An embolus lodged in an artery of the brain results in a stroke. The formation of a thrombus, movement of the embolus, and clogging of an artery is known as a thromboembolism.
Thromboembolisms can arise under various circumstances, and are an acute concern for patients suffering from atrial fibrillation. Atrial fibrillation is the most common cardiac arrhythmia (i.e., abnormal heart rhythm) and involves the two upper chambers (atria) of the heart. Patients suffering from atrial fibrillation normally have a significantly increased risk of stroke because blood may pool and form clots in the poorly contracting atria, and especially in the left atrial appendage (LAA). The LAA is a small cavity that is connected to the lateral wall of the left atrium (LA) between the mitral valve and root of the left pulmonary vein.
With a normal, healthy heart, the LAA contracts with the remainder of the LA during the cardiac cycle, such that blood within the LAA normally is not stagnant. With atrial fibrillation, however, the LAA (as well as the remainder of the LA) may not contract as expected due to the discoordinated electrical signals. Thus, the LAA is the site of thrombus formation in more than 90 percent of cases of thrombi associated with non-valvular atrial fibrillation. Further, if the LA is enlarged, there is an increased risk and percentage of thrombi that originate in the LA. Moderate to severe mitral regurgitation reduces the risk of stroke for the cases of LA enlargement. The LAA lies in close relation to the free wall of the left ventricle and thus the LAA's emptying and filling, which determines this degree of blood stagnation, may be significantly affected by left ventricular function.
To address the risk of stroke, patients suffering from atrial fibrillation are often administered (oral or systemic) anticoagulants or similar pharmacological therapies. Warfarin is a well-accepted anticoagulant, and is commonly given to atrial fibrillation patients to protect them from stroke. Unfortunately, warfarin (also known as coumadin) has some potential adverse side effects including hemorrhaging. The risk of severe hemorrhaging is small but definite, and any benefit needs to outweigh this risk when warfarin is considered as a therapeutic measure. The risk of bleeding is increased when warfarin is combined with antiplatelet drugs such as aspirin. Additionally, patients must remain vigilant in adhering to the prescribed pharmacological therapy regimen.
In light of the above, a need exists for non-pharmacological systems and methods for preventing formation of blood clots in the left atrium (or other cardiac chamber), especially for patients with atrial fibrillation.